SUMMARY: "EFFECTS OF INHALED NITRIC OXIDE IN AN EXPERIMENTAL MODEL OF ONE LUNG VENTILATION" Background: Inhaled nitric oxide (iNO) causes vasodilation and redistribution of pulmonary blood flow (PBF) to ventilated areas in the lung, and this effect can be enhanced by treatments that increase pulmonary hypoxic vasoconstriction (PHV). We hypothesized that during one lung ventilation (OLV) iNO, and the combination of iNO with L-NAME or indomethacine would increase (PBF) to ventilated lung and ameliorate gas exchange. Methods: Twenty six anesthetized adult sheep were included. Lambs were instrumented with a femoral artery catheter, pulmonary artery catheter, electromagnetic blood flow probe in left pulmonary artery and a tracheotomy. After initial measurements left lung ventilation was established. A dose response curve to iNO at 10, 20, 40 and 80 ppm concentrations was first established in seven animals. In the experimental protocol 14 sheep inhaled NO for ten minutes, then they were randomized to receive either L-NAME (30 mg.kg-1) or indomethacine (5 mg.kg-1) i.v. and after a 30 minutes period iNO was administered again. Five animals were followed as a control group. Hemodynamic parameters, PBF in the ventilated lung and arterial and mixed venous gases were obtained before and after each intervention. Results: OLV caused severe hypoxemia in this model (PaO2 60 more/less 9 mmHg).All doses of iNO increased PBF to ventilated lung and oxygenation without dose-response relationship, however more animals responded to the 40 ppm dose. INO at 40 ppm caused selective pulmonary vasodilation, increased both PBF to ventilated lung (11%, p<0.01) and oxygenation (13%, p<0.01). L-NAME severely decreased cardiac output (-30%, p<0.01), increased pulmonary pressure (53%, p<0.01) redistributed PBF and decreased venous admixture (-20%, p<0.01). Combination of iNO and L-NAME caused a synergistic effect in PBF redistribution (65%, p<0.01) and oxygenation improvement (77%, p<0.01). Indomethacine alone caused pulmonary hypertension (22%, p<0.01) without any effect on PBF and gas exchange and did not potentiated the effects of iNO in these parameters. Conclusions: Inhaled nitric oxide improves PBF distribution and oxygenation during severe hypoxemia in this experimental model of OLV. L-NAME administration enhanced PHV in non ventilated lung and clearly potentiated the effects of iNO although high doses of L-NAME cause intense hemodynamic changes.